Management of Acute Kidney Injury in a Patient with Elevated Creatinine
The best next step in this patient with acute kidney injury is to discontinue pantoprazole due to suspected proton pump inhibitor-induced acute tubulointerstitial nephritis. 1, 2, 3
Assessment of Current Renal Function
This 58-year-old man presents with:
- Elevated serum creatinine of 2.1 mg/dL (increased from baseline of 0.9 mg/dL)
- Reduced GFR of 34 mL/min
- Pyuria (10 WBC per field)
- Hematuria (5 RBC per field)
- Leukocytosis (12,000 WBC with 61% neutrophils)
- Low-grade fever (99.8°F)
These findings are consistent with acute kidney injury (AKI), specifically meeting RIFLE criteria for "Injury" with a >2-fold increase in serum creatinine from baseline 4.
Identifying the Cause of AKI
The patient is currently taking pantoprazole for gastric reflux disease. Proton pump inhibitors (PPIs) like pantoprazole are known to cause acute tubulointerstitial nephritis (AIN), which presents with:
- Elevated creatinine
- Pyuria
- Fever
- Leukocytosis
- Recent exposure to the causative medication (typically within weeks to months)
According to the FDA drug label, acute tubulointerstitial nephritis has been observed in patients taking PPIs and may occur at any point during PPI therapy 1. Multiple case reports have documented pantoprazole-induced AIN 2, 3, 5.
Management Algorithm
Discontinue the offending agent (pantoprazole) - This is the critical first step in management
- The FDA label specifically states: "Discontinue pantoprazole sodium and evaluate patients with suspected acute TIN" 1
Evaluate for alternative causes of AKI:
- Pre-renal: Recent volume depletion, hypotension
- Intrinsic: Other nephrotoxic medications, contrast exposure
- Post-renal: Obstruction
Monitor renal function:
- Check serum creatinine every 2-3 days until improvement
- Monitor electrolytes, especially potassium
Consider corticosteroid therapy if no improvement within 3-5 days after drug discontinuation
Provide supportive care:
- Maintain adequate hydration
- Consider one liter of intravenous fluids if evidence of volume depletion
- Avoid other nephrotoxic agents
Rationale for Discontinuing Pantoprazole
Temporal relationship: The rise in creatinine from 0.9 to 2.1 mg/dL suggests AKI developing during the patient's hospitalization, with pantoprazole being a likely contributor.
Clinical presentation: The combination of fever, pyuria, hematuria, and leukocytosis is consistent with drug-induced AIN.
Established causality: Multiple case reports have documented pantoprazole as a cause of AIN 2, 3, 5.
Guideline recommendation: The FDA label explicitly recommends discontinuation of pantoprazole when AIN is suspected 1.
Reversibility: PPI-induced AIN is typically reversible with early discontinuation of the offending agent 2, 5.
Why Other Options Are Not Preferred
Starting temporary antibiotics: While the patient has leukocytosis, there are no clear signs of infection requiring antibiotics. Treating with antibiotics without a clear source would add another potential nephrotoxin.
Ordering ultrasonography: While imaging may be helpful to rule out obstruction, the clinical picture strongly suggests drug-induced AIN, and discontinuation of the offending agent should not be delayed.
Giving IV fluids: While hydration is important in AKI management, addressing the underlying cause (drug-induced AIN) by discontinuing pantoprazole is the priority. Excessive fluid administration without addressing the primary cause could potentially worsen the patient's condition.
Important Considerations
If renal function does not improve after discontinuation of pantoprazole, consider nephrology consultation and possible kidney biopsy.
The KDIGO guidelines recommend monitoring serum creatinine prior to each dose of potentially nephrotoxic medications 4.
PPI-induced AIN can occur at any time during treatment, even after months or years of use 1.
Recovery of renal function may take days to weeks after discontinuation of the offending agent.